STING (Stimulator of Interferon Genes) can recognize cyclic dinucleotides (CDN) in the cytoplasm, and then activate the innate immune response through the cGAS-STING pathway. Currently, agonists targeting STING have garnered significant attention from researchers in the fields of cancer, obesity, viral infections, liver injury, and disorders of lipid and glucose metabolism. The main mechanism of STING in tumors is its involvement in the T-cell-mediated tumor immune process. Activation of the cGAS-STING pathway has been detected to effectively inhibit cancer cell metastasis in various cancer-related diseases such as colorectal cancer, melanoma, and the absence of telomerase.The STING KO Reporter THP1 Cell Line is a luciferase reporter gene cell line constructed based on the STING/TBK1/IRF3 signaling pathway. In this cell line, derived from the STING Reporter THP1 Cell Line, the STING gene is knocked out, meaning CDNs cannot bind to STING and activate the cGAS-STING pathway. However, the use of IFNα can still activate the JAK-STAT pathway, leading to the expression of luciferase. The luciferase reading reflects the activation effect of the signaling pathway and can therefore be used as a control in the STING Reporter THP1 Cell Line to verify the binding specificity of CDN drugs.
